LncRNA HITT Overexpression in Gastric Cancer Promotes Cell Apoptosis by Suppressing the Maturation of miR-602

Abstract Background : HITT inhibits colon cancer. This study explored its role in gastric cancer (GC). Methods : HITT, mature miR-602 and premature miR-602 expression in paired GC and normal tissues (62 patients) was studied by RT-qPCR. RNA pull-down assay was performed to analyze the direct interaction between HITT and mature miR-602. The subcellular location of HITT was analyzed by nuclear fractionation assay. The role of HITT in regulating miR-602 maturation was analyzed by overexpression assay. Cell apoptosis was analyzed by flow cytometry. Result : Our assays illustrated that HITT was highly expressed in GC and mature miR-602 was lowly expressed in GC. No alteration in premature miR-602 in GC was observed. HITT was located to both nucleus and cytoplasm, and it can directly interact with miR-602. HITT overexpression in GC cells increased the expression of mature miR-602 but not premature miR-602. HITT overexpression increased GC cell apoptosis and suppressed the role of miR-602 in inhibiting GC cell apoptosis. Conclusion : Therefore, HITT may promote GC cell apoptosis by suppressing the maturation of miR-602.